Mitchell L Schubert1. 1. Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University's Medical College of Virginia and McGuire VAMC, Richmond, Virginia, USA. Mitchell.Schubert@med.va.gov
Abstract
PURPOSE OF REVIEW: The purpose of this chapter is to summarize and place into perspective the past year's literature regarding the regulation of gastric exocrine and endocrine secretion. RECENT FINDINGS: To prevent acid and pepsin from overwhelming mucosal defense mechanisms and causing injury, the secretion of gastric acid is precisely regulated by a variety of central (eg, neuropeptide Y, corticotropin-releasing factor, and neuromedin U) and peripheral (eg, gastrin, histamine, acetylcholine, somatostatin, cholecystokinin, calcitonin gene-related peptide, leptin, and parietal cell) pathways. These pathways regulate the acid-producing parietal cell directly and/or indirectly by regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and somatostatin from D cells. Recently, genetically engineered mouse models have been used to reevaluate the neural, hormonal, and paracrine pathways that physiologically regulate acid secretion. SUMMARY: An improved understanding of the pathways and mechanisms regulating gastric acid secretion should lead to the development of novel therapies to prevent and treat acid-peptic disorders as well as circumvent the adverse effects of currently used antisecretory medications such as the acid rebound observed after discontinuation of proton pump inhibitors.
PURPOSE OF REVIEW: The purpose of this chapter is to summarize and place into perspective the past year's literature regarding the regulation of gastric exocrine and endocrine secretion. RECENT FINDINGS: To prevent acid and pepsin from overwhelming mucosal defense mechanisms and causing injury, the secretion of gastric acid is precisely regulated by a variety of central (eg, neuropeptide Y, corticotropin-releasing factor, and neuromedin U) and peripheral (eg, gastrin, histamine, acetylcholine, somatostatin, cholecystokinin, calcitonin gene-related peptide, leptin, and parietal cell) pathways. These pathways regulate the acid-producing parietal cell directly and/or indirectly by regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and somatostatin from D cells. Recently, genetically engineered mouse models have been used to reevaluate the neural, hormonal, and paracrine pathways that physiologically regulate acid secretion. SUMMARY: An improved understanding of the pathways and mechanisms regulating gastric acid secretion should lead to the development of novel therapies to prevent and treat acid-peptic disorders as well as circumvent the adverse effects of currently used antisecretory medications such as the acid rebound observed after discontinuation of proton pump inhibitors.
Authors: Modinat A Adefisayo; Rufus O Akomolafe; Stephen O Akinsomisoye; Quadri K Alabi; Olaofe L Ogundipe; Joseph G Omole; Kehinde P Olamilosoye Journal: Toxicol Rep Date: 2017-11-13